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But now we're altering their access to our red blood cells
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Because proteins of the malarial parasite will also become carbamoylated and be less functional. And then of course the sickle cell, if it's not totally sickle cell anemia but sickle cell trait, then it's beneficial in terms of protecting it against malaria.

And there's another enzyme, a glucose-6-phosphate dehydrogenase, which is just a minor enzyme in the hexose monophosphate shunt. As you're driving down the glycolytic pathway, you turn left. And there's the hexose monophosphate shunt. And that G6PD helps to protect the integrity of the cell membrane,

the red blood cell membrane. So it looks as though the diet can also decrease the active form of this enzyme, which also seems to protect against malaria. So this is why we have this pyramid-like triangular figure here, where the diet is influencing not only the human and the metabolic processes of the human,

but also at influencing the parasite-- in this case, Plasmodium falciparum-- that is interested in consuming the same metabolic products from the human. Because the parasite wants the contents of our red blood cell for its own growth and development.

But now we're altering their access to our red blood cells through the diet. That's simply human-plant-parasite co-evolution, where the evolutionary trajectories of all three species are being modified, they're modifying each other, but it's like a symphony all coming together.

So on top of that now, we have the epigenomics. These are the chemicals that surround the genome. And these chemicals can influence gene expression They don't change the gene, but they change gene expression. And it's so fascinating, because it's inherited.

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